The large number of laboratories currently involved defining the physical, functional and molecular characteristics of Ly-1 B (C5D) cells highly recommends this area as an appropriate subject for a meeting organized by the New York Academy of Sciences. Such a meeting, held one to two years from now, would provide a much needed forum for the exchange of information and ideas amongst those researchers actively pursuing Ly-1 B cell studies. In addition, it-would provide a comprehensive and hopefully focussed review of the field that should be of interest and use to a much broader group of clinical and basic immunologists. Ly-1 B cells were first recognized several years ago as a small subset of murine B cells that produces many of the commonly studied autoantibodies and much of the serum Ig in normal and autoimmune animals. Current evidence assigns these cells to a separate developmental lineage that occupies a unique functional niche in the mouse. That is, because this lineage develops its repertoire during neonatal life and persists by self-replenishment in adults, neonatal influences such as antigenic stimulation, idiotypic network interactions and environmental conditions can exert a prolonged effect on the immune system. Thus Ly-1 B cells in effect provide a kind of immunologic memory that keep elements of the neonatal immunologic experience active throughout life. Apparently homologous B cells expressing CD5 (Leu-1) have been found in man. These cells show similar (although not identical) physical, functional and molecular characteristics to their murine counterparts. Clinically, they are of interest because of their extraordinarily high representation in chronic lymphatic leukemia (CLL) and their potential role(s) in immune defenses, in "natural" autoantibody production and in autoimmune diseases such as rheumatoid arthritis, Sjogren's syndrome and perhaps even in AIDS. This meeting will focus on murine Ly-1 B cells but will also include relevant studies on the human Leu-1 B cell repertoire and its relationship to disease.